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Editor,—The British Society of Gastroenterology should be congratulated for commissioning the guidelines on the management of acute pancreatitis (Gut1998;42(suppl 2):S1–13). However, in this document the clinically relevant issue of drug treatment of acute pancreatitis has not been reviewed in depth. Although we agree that current treatment of severe necrotising pancreatitis is unsatisfactory, we do not share the opinion that beyond resuscitation and support there is no agreed specific treatment. We would like remind members of the working party and the experts who have reviewed the document that in two previous meta-analyses, both somatostatin and gabexate mesilate seemed to reduce, respectively, mortality and complications in these patients.1 ,2 Despite this evidence, the use of these drugs has not been recommended or even discussed; based on a single randomised controlled trial in which somatostatin was given for only two days in very small doses, all therapeutic options have been dismissed by the working party as of unproved value.
The authors of the guidelines recognise that as new evidence comes to light, the document will need to be reviewed continuously. A recent meta-analysis has been published in which a total of 25 controlled clinical trials exploring the usefulness of somatostatin (11 studies), octreotide (eight studies), and gabexate mesilate (six studies) in patients with acute pancreatitis has been evaluated. The analysis has shown that the first two agents reduce mortality without affecting complications, and that gabexate mesilate reduces complications but not mortality.3 Given the lack of interaction between this latter agent and somatostatin and octreotide, a future trial exploring the efficacy of combining these drugs might be of great help. Presently, the data in the three meta-analyses constitutes a sound, objective basis on which to tackle therapeutic decisions.
The statement endorsed by the working party seems to reflect the common belief shared by leading authorities in this field that these agents are ineffective in the treatment of acute pancreatitis. This may be because the drugs are believed to act through their antisecretory or protease inhibitory activity. However, other relevant properties of somatostatin and octreotide, namely the haemodynamic effects on reducing splanchnic blood flow, the stimulation of the hepatic reticuloendothelial system, and the modulation of the cytokine cascade, are usually forgotten. It has been hypothesised that the efficacy of somatostatin and octreotide in acute pancreatitis might be better explained by all these properties rather than its capability of inhibiting pancreatic secretion.3